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1. The regular consumption of alcohol elevates blood pressure, with global estimates that the attributable risk for hypertensive disease from alcohol is 16%. 2. The increase in blood pressure is approximately 1 mmHg for each 10 g alcohol consumed and is largely reversible within 2-4 weeks of abstinence or a substantial reduction in alcohol intake. 3. This increase in blood pressure occurs irrespective of the type of alcoholic beverage. In particular, the postulated effects of vasodilator flavonoid components of red wine to lessen or reverse alcohol-related hypertension have not been borne out in intervention studies. 4. Heavy drinking, especially a binge pattern of drinking, is linked to a higher incidence of cerebral thrombosis, cerebral haemorrhage and coronary artery disease deaths, although a role for alcohol-related hypertension in the causal pathway is not well defined. 5. In contrast, the light to moderate intake of alcohol has been consistently linked to a reduced risk of atherosclerotic vascular disease end-points. Such a protective effect may also extend to hypertensive subjects. 6. However, the magnitude of any protective effect appears to have been exaggerated because of unmeasured confounders, especially diet, lifestyle and patterns of drinking. Furthermore, a decrease in overall mortality with drinking appears confined to older subjects and to populations with a high background cardiovascular risk profile. 7. Any putative cardiovascular benefits from drinking need to be carefully considered against the effects of alcohol to elevate blood pressure, together with many other adverse health consequences from drinking. Maximum cardiovascular benefit occurs at relatively low levels of consumption (i.e. one to two standard drinks a day in men (10-20 g alcohol) and up to one a day in women (10 g alcohol)). In hypertensive subjects, consumption beyond these levels would be unwise.

1. Oscillometric devices for blood pressure (BP) measurement at the wrist are becoming more widely used in clinical practice. However, systematic comparisons with standard auscultatory BP measurement at the brachial artery are scarce. Therefore, we compared two such devices, the Boso-Mediwatch (Bosch & Sohn GmbH U. Co., Jungingen, Germany) and the Omron R3 (Omron Corp., Tokyo, Japan), with upper-arm auscultatory mercury sphygmomanometry. 2. In 20 normotensive subjects and 20 treated hypertensive subjects, the Boso-Mediwatch was applied to the left wrist by observer 1 and was compared with mercury sphygmomanometry of the right upper arm by observer 2. Each observer swapped sides and the procedure was repeated. The Boso-Mediwatch was then applied to the right wrist by observer 1 and was compared with mercury sphygmomanometry of the left upper arm by observer 2. Each observer once again swapped sides and the procedure was repeated. An identical protocol was followed for the Omron R3 in a further 20 treated hypertensive subjects and 20 normotensive subjects. 3. There were no significant differences between observers or left versus right arm for either oscillometric device or when measurements were performed by mercury sphygmomanometry. In normotensive subjects, the Boso-Mediwatch readings were higher than mercury sphygmomanometer readings, with mean differences (95% confidence intervals) of 3.9 (0.1, 7.6; P = 0.045) and 7.0 mmHg (4.7, 9.2; P < 0.001) for systolic and diastolic BP, respectively. In hypertensive subjects, the Boso-Mediwatch readings were lower for systolic BP (mean difference -6.0 mmHg (-11.6, -0.3; P = 0.04) but were higher for diastolic BP (mean difference 3.8 mmHg (1.4, 6.3; P < 0.01). 4. In normotensive subjects, the Omron R3 readings were higher, with mean differences of 3.2 (0.6, 5.8; P = 0.018) and 4.2 mmHg (1.6, 6.7; P = 0.003) for systolic and diastolic BP, respectively. In hypertensive subjects, the Omron R3 readings were lower for both systolic and diastolic BP (mean differences: -5.8 (-8.8, -2.8; P = 0.001) and -5.5 (-9.3, -1.6; P = 0.008), respectively). 5. For the Boso-Mediwatch, weighted least products analysis confirmed the presence of both fixed and proportional error for systolic BP but not for diastolic BP. For the Omron R3, fixed or proportional error was not detected for either systolic or diastolic BP. 6. These wrist oscillometric devices, although offering portability and convenience, give BP measurements that frequently differ substantially (by at least 5 mmHg) from readings simultaneously measured at the upper arm by a mercury sphygmomanometer. The magnitude and direction of differences detected are dependent on both the device used and the underlying level of BP.

SUMMARY 1. Changes in membrane fluidity have been proposed to contribute to the pathogenesis of ethanol-induced hypertension possibly through changes in membrane lipid patterns, but reports are inconsistent. 2. In a controlled trial we documented ethanol-induced changes in blood pressure and composition of membrane lipids in ethanol-fed rats. 3. Systolic blood pressure increased significantly in the ethanol-treated rats (9.3 mmHg, s.e.m. 2.9) compared with the control group (- 1.3 mmHg, s.e.m. 2.6). Mean cholesterol content in red cell membranes did not differ significantly between ethanol-fed and control rats. Phospholipids of aorta, red cells and kidney showed a significant decrease in the polyunsaturated to saturated fatty acid ratio, while membrane phospholipids from the heart showed a significant increase in the polyunsaturated to saturated fatty acid ratio with ethanol treatment. 4. In univariate regression blood pressure was significantly negatively related to levels of arachidonic acid in the kidney (P = 0.0013) and to linoleic acid in the aorta (P = 0.0341) and red cells (P = 0.0289). Blood pressure was not significantly related to fatty acids in the heart nor to membrane cholesterol or phospholipids. 5. Differences in fatty acid composition of phospholipids between controls and ethanol-fed rats are consistent with altered membrane fluidity. Altered membrane function is a potential mechanism involved in ethanol-induced hypertension.

1. We have conducted a survey of 75 rural and 75 urban randomly selected general practioners (GPs) in Western Australia to ascertain how closely current practice mirrors published Australian guidelines for the management of hypertension. 2. Fifty-one rural and 49 urban GPs completed the 19 item questionnaire. The two groups were well matched in terms of age and years in general practice. An assessment of the criteria utilized to diagnose hypertension revealed a tendency for much greater scatter in the cut points used to define systolic compared to diastolic hypertension, but no systematic difference between urban and rural GPs. 3. After an initial finding of mild hypertension the follow-up time to the next check-up was significantly longer for rural patients compared to urban patients (72 +/- 13 and 36 +/- 5 days respectively, P < 0.01). Urban GPs reviewed established hypertensive patients more commonly at 1-3 monthly intervals (89%) while rural GPs reviewed more commonly at 3-6 monthly intervals (86%). 4. In terms of target blood pressure (BP) for BP reduction, 67% rural compared to 83% urban GPs aimed for a systolic BP of < 140 mmHg (P = 0.06), while 95% of both groups aimed for diastolic BP < 90 mmHg. 5. The profile of first line antihypertensive agents most commonly used was also similar in both groups with 46% preferring angiotensin converting enzyme inhibitors, 18.5% diuretics, 18.5% beta blockers, 16% calcium entry blockers and 1% prazosin. 6. This study demonstrates a clear preference for the newer anti-hypertensive agents.(ABSTRACT TRUNCATED AT 250 WORDS)

SUMMARY 1. From an earlier cross-sectional survey of 343 public servants, 15 pairs of non-smoking teetotallers and heavy drinkers (alcohol intake more than 350 mL/week) were matched for age and adiposity and utilized for a case-control study of the effects of alcohol on 11β-hydroxysteroid dehydrogenase (11β-OHSD) activity and blood pressure. 2. Two successive 24 h urine collections were analysed by radio-immunoassay (RIA) for cortisol excretion, and for the cortisol and cortisone metabolites, tetrahydrocortisol (THC), allo-tetrahydrocortisol (allo-THC) and tetrahydrocortisone (THE), by capillary column gas chromatography. 3. Heavy drinkers had higher systolic and diastolic blood pressure (BP) than teetotallers (132.6 ± 2.5 vs 123.2 ± 1.3 and 78.7 ± 1.6 vs 71.7 ± 1.4, respectively; unpaired t-test, P

SUMMARY 1. To investigate the effect of an exercise training programme on antihypertensive drug requirements, 19 sedentary subjects (14 men and five women) with mild essential hypertension (systolic blood pressure greater than 140 mmHg but less than 180 mmHg), aged 29–55 years, were randomly assigned to 16 weeks of moderate intensity exercise or light intensity exercise (control), and titrated on antihypertensive drug therapy (captopril and hydrochlorothiazide) until resting systolic blood pressure (sitting) of less than 140 mmHg was achieved. 2. The moderate exercise group (n= 11) followed a graded walk-jog programme to >60% age-predicted maximum heart rate (HRmax), attending 45 min sessions, three times each week. The light exercise group (n= 8) followed a programme of flexibility (stretching exercises) and walking to

Forty-four males with treated essential hypertension and a moderate-to-heavy alcohol intake participated in a randomized controlled crossover trial of the effects of varying alcohol intake on blood pressure control. Usual antihypertensive therapy was maintained unchanged throughout. Self-reported alcohol consumption fell from 452 ml ethanol/week (s.e.m. = 29) during normal drinking habits to 64 ml/week (s.e.m. = 8) while drinking low alcohol content beer. Mean systolic and diastolic blood pressures were significantly lower during the last 2 weeks of reduced alcohol (supine 5.0 mmHg, s.e.m. = 1.4, and 3.0 mmHg, s.e.m. = 0.9, respectively; erect 5.9 mmHg, s.e.m. = 1.6, and 2.9 mmHg, s.e.m. = 1.0, respectively). Body weight was also lower (0.94 kg, s.e.m. = 0.25) at the conclusion of the low alcohol intake period. Regression analysis suggested that reduction in alcohol intake contributed independently to the fall in both systolic and diastolic blood pressure, while weight change contributed independently to the fall in systolic blood pressure alone. It was concluded that curtailing moderate to heavy alcohol intake leads to improved blood pressure control in treated essential hypertensive males.

Sulphate conjugation represents an efficient mechanism for inactivating catecholamines (CA) with more than 80% of total noradrenaline (NA) and adrenaline (A) and nearly 100% of dopamine (DA), circulating as conjugates. Sulphate conjugation responds rapidly to changes in sympathetic activity and may buffer the haemodynamic and metabolic consequences of wide fluctuations in CA release in phaeochromocytoma. This hypothesis was tested in seven patients with phaeochromocytoma by consecutive measurements of plasma free and conjugated NA, under resting conditions, before operation and at least 4 weeks after tumour removal. Free and total (free plus sulphates) NA were markedly elevated before (4.3, s.e.m. = 1.8 and 13.7, s.e.m. = 4.4 ng/ml, respectively) compared with 1-4 months after surgery (0.48, s.e.m. = 0.13 and 1.8, s.e.m. = 0.53 ng/ml). A and DA were similarly elevated before surgery; after surgery, A was undetectable in three patients and DA was undetectable in all patients. Before surgery consecutive measurements of total NA, 5 min apart, were markedly different (18.8, s.e.m. = 4.8 and 12, s.e.m. = 3.1 ng/ml, respectively), whereas only small differences in free NA levels were present (4.0, s.e.m. = 1.5 and 4.4, s.e.m. = 1.8 ng/ml). In three patients, fluctuations in total NA concentration greater than 12 ng/ml were associated with either no change (one patient) or changes of 0.6 and 2.8 ng/ml in levels of free NA, respectively. Mean blood pressure varied less than 8 mmHg in these patients. These findings indicate that sulphate conjugation is a dynamic process which may limit wide fluctuations in free CA concentration during episodic secretory activity in phaeochromocytoma.

SUMMARY 1. In a population-based study of 343 men from two public utilities, 260 subjects reported drinking alcohol at least once a week. In these subjects a comparison was made of the relative effects on blood pressure of either their usual alcohol intake (assessed from a 7-day retrospective diary) or recent alcohol intake (alcohol consumed at the last drinking session in the 24 h prior to blood pressure measurement). 2. Both usual and recent alcohol intake showed similar correlations with level of blood pressure (BP). After adjustment of BP for the potential confounding influences of body mass index, age and smoking status, systolic and diastolic BP remained highest in those subjects with the highest reported levels of both usual and recent alcohol intake. 3. In regression analyses comprising only those subjects who reported drinking in the 24 h before BP measurement, a 3–4 fold greater effect of usual rather than recent intake on both systolic and diastolic BP was predicted from the b coefficients. Regression analysis also demonstrated that the relationship between usual alcohol intake and BP was independent of recent intake, while the relationship between recent intake and BP was no longer significant when usual alcohol intake was entered into the regression equation. 4. These observations suggest that consistent regular drinking is a more important determinant of the alcohol/BP relationship than intake in the previous 24 h.